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Activate the gut–adipose Axis: Forsythia tea alleviates diet-induced obesity via gut microbiota–dependent Browning of white adipose tissue
This study investigated the mechanisms by which Forsythia tea (FT) alleviates diet-induced obesity via the gut-adipose axis. Following 8 weeks of high-fat diet (HFD) feeding to induce obesity in male C57BL/6 J mice, the HFD-fed mice were randomized into HFD and HFD + FT groups, with a normal diet (ND) group as control, for a subsequent 4-week intervention. The results demonstrated that FT significantly attenuated HFD-induced body weight gain and improved glucose tolerance and insulin sensitivity. Furthermore, FT effectively reversed dyslipidemia and suppressed systemic inflammation. Mechanistically, FT reshaped the gut microbiota, enhancing alpha diversity and enriching beneficial taxa. These microbial changes were associated with increased colonic short-chain fatty acid (SCFA) levels, particularly butyrate, and reinforced intestinal barrier integrity. Crucially, FT treatment markedly upregulated the expression of uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) in inguinal white adipose tissue (iWAT), indicating the activation of WAT browning. Correlation analyses strongly linked the enriched beneficial microbes to the improved metabolic phenotypes. In conclusion, our findings reveal that FT mitigates obesity and metabolic dysfunction by activating a microbiota-dependent gut-adipose axis that promotes WAT browning, supporting its potential as a functional beverage for obesity management
AI based multiomics integration for cancer diagnosis and prognosis
Cancer remains a critical global health challenge, driving the need for innovative approaches in diagnosis and treatment. This research introduces OmicsFusionNet, an AI-powered hybrid model integrating machine learning and deep learning to revolutionize cancer care. The tool incorporates up to six multiomics datasets—genomics, transcriptomics, and epigenomics—achieving 80.2% accuracy across 23 cancer types. Notably, RNAseq and methylation integration reached 99.8% accuracy, highlighting XGBoost’s feature selection and deep learning’s classification strength.For ovarian cancer stage detection, OmicsFusionNet optimized analysis using CPTAC-OV and TCGA-OV datasets, achieving accuracies between 83% and 91% by combining ElasticNet and XGBoost with deep learning. Additionally, KEGG pathway enrichment of multiomics biomarkers identified key cancer-related pathways, advancing early detection, biomarker discovery, and personalized treatments.This study underscores the transformative potential of AI and multiomics integration in cancer research, enabling precise interventions and uncovering novel mechanisms that enhance patient outcomes
Ultrasound and microwave assisted extraction of bioactives from food wastes: An overview on their comparative analysis towards commercialization
Valorizing food waste to functional bioactives is a robust research area. Sustainability, cost effectiveness, enhanced productivity of the bio-extracts and finally on the industrial readiness have been the driving force for research towards non-thermal extractions, novel solvents, process optimization, dual technological adoption and lately on the use of Artificial Intelligence (AI)/Machine Learning (ML). Ultrasound assisted extraction (UAE) and Microwave assisted extraction (MAE) stand apart in the context of cost-effectiveness and hold tremendous potential to be scaled-up despite the identified challenges.Thus, with the focus on technological merit, scalability challenges, advancements, quality assessment, the present review has made an elaborate performance assessment for bioactive recovery with respect to productivity, green solvents as well as on environment and energy impact. Finally, research and development on AI tools in quality process control, optimization and real-time monitoring and combined use of UAE + MAE in addressing technological flaws, boosting quality, productivity show positive aspects towards commercialization
Red cabbage anthocyanin-rich natural colorant: Optimization of ultrasound-assisted extraction, microencapsulation, bioaccessibility, and functional yogurt development
Anthocyanins from red cabbage (Brassica oleracea var. capitata f. rubra) are promising natural pigments with notable health benefits, but their thermal and gastrointestinal instability limits functional food applications. This study employed ultrasound-assisted extraction (UAE) and spray-drying microencapsulation to enhance their stability, bioaccessibility, and functionality. Optimization using a Box–Behnken design (pH 3.0–5.0, 30–60 °C, 20–90 min, 0.025–0.05 g/mL solid–liquid ratio) identified optimal UAE conditions (pH 3.5, 45 °C, 55 min, 0.0375 g/mL), yielding 125.72 ± 0.83 mg/L anthocyanins. Freeze drying retained the highest anthocyanin content (129.02 ± 3.36 mg/L), while spray-drying with 10 % maltodextrin achieved excellent encapsulation efficiency (96.36 ± 0.80 %) and yield (99.40 %). FTIR confirmed the presence of phenolic groups, and SEM revealed spherical microcapsules (∼10.27 µm) with smooth surfaces. Encapsulation significantly improved thermal stability at 70 °C, reducing the degradation rate constant (0.00043 min−1) and increasing half-life (1919.02 min), compared to non-encapsulated samples. During simulated digestion, bioaccessibility of encapsulated anthocyanins was lower in the oral (53.28 %) and intestinal (25.37 %) phases than free forms, but stability was enhanced. Antioxidant activity (DPPH: 66.90 %, ABTS: 71.76 %) and enzyme inhibition (α-amylase IC50: 46.00 µg/mL, α-glucosidase IC50: 51.51 µg/mL) indicated potent bioactivity. Cytotoxicity testing on HEK-293 cells showed > 90 % viability, confirming safety. Yogurt fortified with 3 % encapsulated powder received high sensory scores (8.30 ± 0.86), especially for color and taste. These findings validate the integrated UAE and encapsulation approach as a scalable method to stabilize red cabbage anthocyanins for functional food applications
Prevalence and correlates of anal HPV infection among men who have sex with men in Brazil: A respondent-driven sampling study
Objectives: Human papillomavirus (HPV) is the main cause of anal carcinoma, whose incidence is rising globally, especially among men who have sex with men (MSM). This study estimated anal HPV prevalence, investigated genotype distribution, and identified associated factors among MSM in Brazil. Methods: The SMESH study, a multicenter cross-sectional survey (2019-2023), analyzed 1375 MSM (≥18 years) from nine Brazilian capitals using respondent-driven sampling. Participants completed questionnaires and provided self-collected anal samples for HPV detection. Weighted analyses were applied. Results: Anal HPV prevalence was 72.4% (95% CI: 67.6-77.3), with 62.3% (95% CI: 56.9-67.8) harboring high-risk HPV and 36.4% (95% CI: 30.9-41.8) infected with quadrivalent vaccine types. MSM living with HIV (18.1%), compared to HIV-negative MSM, had higher overall (87.7% vs 69.6%, P < 0.001) and high-risk HPV prevalence (78.9 vs 58.9%, P < 0.001). Vaccinated MSM presented lower rates of quadrivalent vaccine types, particularly HPV 16. Younger age (25-34 years), frequent group sex, and regular drug use during sex were associated with HPV infection. Conclusion: The high prevalence of anal HPV among Brazilian MSM highlights the importance of expanding HPV vaccination coverage, particularly for HIV-positive MSM, and reinforces the need for gender-neutral vaccination of all girls and boys before sexual debut
Association of anti-interferon antibodies with severe clinical outcomes in West Nile virus: Results of a recent outbreak
Objective: To assess whether anti-interferon (anti-IFN) autoantibodies are associated with more severe clinical and laboratory outcomes in West Nile virus (WNV) patients. Methods: We prospectively evaluated 19 patients diagnosed with WNV during a 2024 outbreak. Serum anti-IFN autoantibodies were measured using a luciferase-based neutralization assay. Patients were stratified into two groups: high anti-IFN levels (n = 5) and normal levels (n = 14) compared to controls (n = 18). Clinical features, neurologic findings, laboratory values, and outcomes were compared. Results: Patients with elevated anti-IFN antibodies had significantly more severe disease. Cerebrospinal fluid (CSF) analysis revealed markedly higher white blood cell counts (712 vs 73 cells/µL, P = 0.02), a higher percentage of polymorphonuclear leukocytes (PMN, 24 vs 72%, P = 0.009), and elevated protein levels (74 vs 98 mg/dL). C-reactive protein (CRP) was also higher (1.23 vs 8.6 mg/dL). Neurological manifestations, including cranial nerve palsy, motor symptoms, and meningitis, were more common. Rash occurred more frequently (60% vs 21.4%). Clinical cure was less frequent (60% vs 100%), and while most patients in the normal antibody levels group were discharged home, none were in the high antibody group. Mortality was 40% vs 21.4%. Conclusion: Elevated anti-IFN antibodies were associated with increased neuroinflammation and worse outcomes. These findings support their potential role as prognostic biomarkers in WNV infection
Tri-modal assessment reveals early visual pathway degeneration in patients with MSA-C
Background and objectives: Post-mortem evidence suggests neurodegeneration in the visual pathway in multiple system atrophy-cerebellar type (MSA-C), yet robust in vivo evidence remains scarce. This study aimed to characterize these visual pathway changes in MSA-C patients by integrating optical coherence tomography (OCT), visual evoked potential (VEP), and magnetic resonance imaging (MRI). Methods: This cross-sectional study prospectively recruited 156 participants, including 53 healthy controls and 103 early-stage MSA-C patients (mean disease duration: approx. 2 years). All participants underwent retinal layer evaluation using OCT. A randomly selected subset of 34 MSA-C patients and 19 controls also received VEP and MRI to assess visual pathway structure and function comprehensively. Results: OCT analysis revealed significant parafoveal thinning within the 3-mm inner ring in MSA-C patients, predominantly affecting the ganglion cell layer (GCL) (P < 0.001) and inner plexiform layer (IPL) (P < 0.001). VEP recordings demonstrated significantly prolonged P100 latency (P < 0.001). MRI confirmed reduced cerebellar volume (P < 0.001). DTI detected microstructural degeneration in the cerebellum and visual pathways, with increased mean and axial diffusivity in optic tracts and radiation. Notably, retinal thinning correlated significantly with longer P100 latency (GCL: r = 0.49, P = 0.003; IPL: r = 0.41, P = 0.015) and cerebellar atrophy (GCL: r = 0.53, P = 0.001; IPL: r = 0.49, P = 0.003), indicating integrated visual pathway degeneration. Conclusions: This large-scale multimodal study provides robust in vivo evidence that MSA-C involves early retinal neurodegeneration, functional conduction delay, and central white matter degeneration. The convergence of OCT, VEP, and DTI parameters suggests bidirectional retinocortical degeneration. Our findings support the potential of these parameters for early detection and highlight the visual pathway as a promising potential biomarker in synucleinopathies
Protrudin acts at ER-endosome contacts to promote KIF5-mediated endosomal tubule fission
Defective endosomal sorting and trafficking are increasingly recognised as key drivers of neurodegeneration, including hereditary spastic paraplegia (HSP) and other motor neuron disorders. Early endosomal tubule fission (ETF) is essential for sorting cargoes for recycling and retrograde transport, yet the mechanisms coordinating this process are incompletely defined. Here, we identify the endoplasmic reticulum (ER)–resident protein protrudin—previously shown to promote axonal regeneration after injury—as a key regulator of ETF. Using CRISPR interference in human cells, we show that loss of protrudin causes marked accumulation of elongated endosomal tubules, caused by defective fission. Protrudin-mediated ETF required its ability to interact with ER-localised VAP proteins, endosomal phosphoinositides, and the kinesin motor KIF5, indicating a function at ER–endosome contact sites. The endosomal tubulation phenotype depended on dynamic microtubules and dynein and was phenocopied by KIF5 depletion, suggesting that protrudin coordinates opposing microtubule motor forces to drive fission. Beyond this direct role, protrudin connects multiple ETF machineries implicated in lipid transfer, actin regulation, and ER shaping, positioning it as a central scaffold for ETF. Importantly, depletion of protrudin or the HSP-associated kinesin KIF5A produced similar endosomal tubulation defects in human cortical neurons, underscoring the neurophysiological and disease relevance of this pathway. These findings identify protrudin as a key molecular link between ER–endosome communication, neuronal membrane trafficking, and axonal maintenance—processes whose disruption underlies neurodegenerative disease
Transcriptomic and neurotransmitter correlates of structure and function spatial variations patterns in spinocerebellar Ataxia
Background: Spinocerebellar ataxia (SCA) is characterized by cortical structural and functional impairments, but the underlying biological mechanisms remain poorly understood. Methods: We applied T1-weighted magnetic resonance imaging (MRI) and resting-state functional MRI (fMRI) to investigate cortical alterations in 49 SCA patients and 48 matched controls. Cortical thickness and amplitude of low-frequency fluctuations (ALFF) were quantified and compared with spatial maps of 19 neurotransmitter systems. Gene expression patterns were examined using partial least squares regression, followed by gene ontology analysis to identify associated biological processes. Results: Both cortical thickness and ALFF emerged as sensitive biomarkers of cortical impairment in SCA. Thickness alterations were strongly associated with disruptions in cholinergic, serotonergic, and glutamatergic systems. ALFF alterations were linked to toxin-response and detoxification processes, with relevant gene expression enriched in astrocytes. Conclusion: Our convergent imaging–transcriptomic analysis integrates direct molecular vulnerability and CTC-based transsynaptic degeneration, yielding a unified systems-level view of SCA. These findings go beyond correlation by prioritizing molecular pathways and non-neuronal cellular targets and enabling network-informed prediction of additional vulnerable regions
Integrated peripheral metabolic and inflammatory biomarker signatures are associated with clinical deterioration in Creutzfeldt–Jakob disease
Introduction: Systemic metabolic and inflammatory disturbances are implicated in neurodegenerative diseases, but comprehensive metabolomic profiling in Creutzfeldt–Jakob disease (CJD) remains limited, and the potential interplay between peripheral metabolism and inflammatory or tissue-remodeling processes is poorly understood. Objectives: This study aimed to characterize the plasma metabolome and inflammatory/proteolytic profile in CJD, and to evaluate their individual and combined associations with cerebral glucose metabolism and clinical severity. Methods: From January 2020 to July 2023, we recruited patients with probable or definite genetic CJD and age- and sex-matched healthy controls (HCs) at Xuanwu Hospital. All participants underwent plasma metabolomic profiling, cytokine testing, brain 18F-FDG PET/MRI, and clinical assessments. Orthogonal projections to latent structures-discriminant analysis (OPLS-DA) identified differentially abundant metabolites (variable importance in projection >1, p < 0.05). Linear and interaction models, adjusted for age and sex, evaluated associations with cerebral hypometabolism and clinical outcomes. Results: We enrolled 40 CJD patients (mean age 60.8 years, 42.5 % female) and 40 HCs. OPLS-DA revealed clear separation between groups, and 42 differentially abundant metabolites were identified from the initial 163 metabolites that differed between groups. Enrichment analysis revealed dysregulation in metabolic pathways related to amino acid biosynthesis, alanine, aspartate and glutamate metabolism, ABC transporters, glycerophospholipid metabolism, and others. Levels of IL-4, IL-18, IL-22, IFN-γ, IL-1β, IL-6, MMP-1, and MMP-8 were significantly elevated in CJD patients. Multiple metabolites and these peripheral factors correlated with hypometabolism in vulnerable brain regions and with cognitive and functional decline. Interaction analyses further showed that specific metabolite–mediator combinations (e.g., Glycerophosphocholine, Glyceric acid, Asparagine, Dimethylglycine, 3-Phosphoglycerate with IL-1β, IL-4, IL-6, IL-22, MMP-8) were significantly associated with regional hypometabolism and clinical deterioration. Conclusion: CJD involves coupled peripheral metabolic and inflammatory/proteolytic disturbances that may be associated with more severe brain degeneration and clinical decline, suggesting a possible multifaceted systemic component accompanying disease pathology